A peptide of the N terminus of GRK5 attenuates pressure-overload hypertrophy and heart failure
Ryan C. Coleman, Akito Eguchi, Melissa Lieu, Rajika Roy, Eric W. Barr, Jessica Ibetti, Anna Maria Lucchese, Amanda Peluzzo, Kenneth S. Gresham, J. Kurt Chuprun, Walter J. Koch
Abstract
-CaM from associating with endogenous GRK5, thereby preventing GRK5 nuclear accumulation after pressure overload. We generated mice that expressed GRKnt in a cardiac-specific fashion (TgGRK5nt mice), which exhibited reduced cardiac hypertrophy, ventricular dysfunction, pulmonary congestion, and cardiac fibrosis after chronic transverse aortic constriction. Together, our data support a role for GRK5nt as an inhibitor of pathological GRK5 signaling that prevents heart failure.
Topics & Concepts
Pressure overloadHeart failureChromosomal translocationMuscle hypertrophyPathologicalInternal medicineMedicineCell biologyPeptideBiologyCardiac hypertrophyCardiologyBiochemistryGeneReceptor Mechanisms and SignalingCardiac electrophysiology and arrhythmiasSignaling Pathways in Disease